作者: María J. López-Armada , Marta N. Valcárcel-Ares , Romina R. Riveiro-Naveira , Carlos Vaamonde-García
DOI: 10.1007/978-1-4614-6166-1_3
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摘要: Mitochondrial characteristics, including mitochondrial respiratory chain (MRC) activity, ATP synthesis, and membrane potential (∆ψm), are altered in osteoarthritis (OA) chondrocytes the synovium of inflammatory arthritis, or synovial cells under arthritic-like conditions, suggesting a role dysfunction these types arthritis. Nitric oxide (NO) is an mediator produced large amounts at sites inflammation, rheumatic joint tissues. Most catabolic effects NO synoviocytes potentially related to ability combine with superoxide anion (O2 −) generate peroxynitrite (ONOO−), very strong oxidant capable inhibiting important enzymes affecting integrity. Oxidative mtDNA damage caused by mutagens such as reactive oxygen nitrogen species could be main source genomic instability that leads dysfunction. NO-induced may explain several events involved pathogenesis chronic arthropathies OA rheumatoid arthritis (RA).